Correlation between airway hyperresponsiveness and airway inflammation in a young adult population: eosinophil, ECP, and cytokine levels in induced sputum
Y. Obase et al., Correlation between airway hyperresponsiveness and airway inflammation in a young adult population: eosinophil, ECP, and cytokine levels in induced sputum, ANN ALLER A, 86(3), 2001, pp. 304-310
Background: Eosinophil counts and eosinophil cationic protein (ECP) levels
in the airway are elevated in asthmatic patients. However, few studies have
examined the correlation between various cytokines in the sputum and airwa
y hyperresponsiveness (AHR) in young adults with or without asthma.
Objective: We examined the correlation between AHR and eosinophil counts or
ECP, and levels of several cytokines in the sputum.
Methods: We studied 120 nonsmoker students (group 1: intermittent mild asth
matic patients; group 2: subjects with history of childhood asthma; group 3
: subjects sensitized by Dermatophagoides farinae with atopic disease; grou
p 4: normal subjects sensitized by D. farinae; group 5: subjects with cedar
pollinosis; and group 6: normal subjects). In each subject, AHR and lung f
unction tests were measured, together with eosinophil count, ECP, granulocy
te-macrophage colony-stimulating factor, TNF-alpha, IL-5, and interleukin-1
beta in induced sputum.
Results: AHR in groups 1 and group 2 were high, in groups 5 and 6 low, and
in groups 3 and 4 lower than in groups 1 and 2 but higher than groups 5 and
6. Percentages of eosinophils, ECP, and TNF-alpha in induced sputum in gro
ups 1 and 2 were high, those in groups 5 and 6 were below detection limits,
and those in groups 3 and 4 were lower than the percentages in groups 1 an
d 2. Granulocyte-macrophage colony-stimulating factor in the sputum was ele
vated only in group 1. The correlations between AHR and sputum eosinophil c
ount, ECP, and TNF-alpha were significant, with the strongest correlation w
ith TNF-alpha.
Conclusions: Our results suggest that TNF-alpha levels in the sputum play a
n important role in determining the severity of AHR in young individuals. F
urther once AHR develops, it does not disappear, and the severity of airway
inflammation influences the extent of AHR.